LncRNA TUG1 contributes to cardiac hypertrophy via regulating miR-29b-3p

Zou, Xingxing; Wang, Jialiang; Tang, Li; Wen, Qian

doi:10.1007/s11626-019-00368-x

Cited by 26 publications

(18 citation statements)

References 38 publications

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“…TUG1 had been found to play a crucial role in hypoxia-induced myocardial cell damage via regulating B-cell lymphoma 2 interacting protein 3 (Binp3) by sponging miR-145-5p [25]. In the current study, our data demonstrated that TUG1 was upregulated in the TAC rat model and Ang II-induced cardiomyocytes, and TUG1 knockdown attenuated Ang II-induced cardiomyocyte hypertrophy in agreement with the previous study [10].…”

Section: Discussionsupporting

confidence: 92%

“…Wang et al identified that cardiac hypertrophy-associated epigenetic regulator (Chaer) worked as an epigenetic checkpoint in cardiac hypertrophy [9]. A recent study demonstrated that taurine upregulated gene 1 (TUG1) was involved in the pathogenesis of cardiac hypertrophy by sponging miRNA-29b-3p [10]. Herein, we identified the functional role and the underlying mechanisms of TUG1 in cardiac hypertrophy.…”

Section: Introductionmentioning

confidence: 87%

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Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis

Zhang

2021

Open Life Sciences

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The aim of this study was to investigate the detailed role and molecular mechanism of long noncoding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in cardiac hypertrophy. Cardiac hypertrophy was established by transverse abdominal aortic constriction (TAC) in vivo or angiotensin II (Ang II) treatment in vitro. Levels of lncRNA TUG1, miR-497 and myocyte enhancer factor 2C (MEF2C) mRNA were assessed by quantitative reverse transcriptase PCR (qRT-PCR). Western blot assay was performed to determine the expression of MEF2C protein. The endogenous interactions among TUG1, miR-497 and MEF2C were confirmed by dual-luciferase reporter and RNA immunoprecipitation assays. Our data indicated that TUG1 was upregulated and miR-497 was downregulated in the TAC rat model and Ang II-induced cardiomyocytes. TUG1 knockdown or miR-497 overexpression alleviated the hypertrophy induced by Ang II in cardiomyocytes. Moreover, TUG1 acted as a sponge of miR-497, and MEF2C was directly targeted and repressed by miR-497. miR-497 overexpression mediated the protective role of TUG1 knockdown in Ang II-induced cardiomyocyte hypertrophy. MEF2C was a functional target of miR-497 in regulating Ang II-induced cardiomyocyte hypertrophy. In addition, TUG1 regulated MEF2C expression through sponging miR-497. Knockdown of TUG1 rescued Ang II-induced hypertrophy in cardiomyocytes at least partly through targeting the miR-497/MEF2C axis, highlighting a novel promising therapeutic target for cardiac hypertrophy treatment.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 87%

Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis

Zhang

2021

Open Life Sciences

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“…Additionally, TUG1 promotes cancer progression through accelerating cell proliferation and inhibiting cell apoptosis (Kuang, Zhang, Hua, Dong, & Li, 2016; Li, Chen, Zhang, & Liu, 2018; Li, Zhang, Liu, & Chen, 2018). It has also been reported that TUG1 promotes multiple myeloma cell proliferation and inhibits apoptosis by suppressing miR‐29b‐3p (Liu, Wang, & Liu, 2019), and TUG1 induces cardiac hypertrophy through sponging miR‐29b‐3p (Zou, Wang, Tang, & Wen, 2019). Moreover, TUG1 promotes OC cell proliferation and invasion by regulating WNT/β‐catenin pathway (Liu, Liu et al, 2018), or regulates angiogenesis by regulating expression of LRG1 (Fan, Li, et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Long noncoding RNA TUG1 facilitates cell ovarian cancer progression through targeting MiR‐29b‐3p/MDM2 axis

Yang

Xin

et al. 2020

The Anatomical Record

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Ovarian cancer (OC) is one of the most aggressive female cancers in the world. OC trends to be diagnosed at an advanced stage with abdominal metastasis. Our study explored the biological function and underlying mechanism of lncRNA on OC cell proliferation and migration. The expression of turine upregulated gene 1 (TUG1) in human OC tissues and cell lines was measured by qRT-PCR. OC cell proliferation, viability, migration, and invasion were measured by MTT assays, colony formation assays, and transwell assays in vitro. Furthermore, the nude mice xenograft model was established to determine the effects of TUG1 in vivo. The relationship between TUG1 and miR-29b-3p, as well as miR-29b-3p and MDM2 were identified using the luciferase reporter assays. We showed that the expression of TUG1 and MDM2 were significantly increased, but the expression of miR-29b-3p was remarkably decreased in OC tissues and cell lines. Knockdown of TUG1 strongly inhibited the ability of cell proliferation, colony formation, migration, and invasion in vitro. The relationship between TUG1 and miR-29b-3p, or miR-29b-3p and MDM2 were predicted by StarBase and miRanda online software. Besides, miR-29b-3p reversed the positive effect of TUG1 on the OC cell proliferation, migration, and invasion through inhibiting MDM2 expression and increasing p53 phosphorylation level. Moreover, knockdown of TUG1 suppressed tumor growth in vivo. Taken all together, this study shows that TUG1 plays a crucial oncogenic role and facilitates cell proliferation, migration, and invasion in OC through regulating miR-29b-3p/MDM2 axis.

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“…These data suggested that NT-proBNP may be used as one of the hematological diagnostic indexes for hypertensive patients with HFPEF. As a novel lncRNA, TUG1 has been reported to participate in the development of cardiac diseases, including cardiac hypertrophy (21), ischemic myocardial injury (22) and atherosclerosis (23). Therefore, in the present study, the role of TUG1 in HF was investigated and it was determined that the serum levels of TUG1 in hypertensive patients with HFPEF were significantly higher than those in hypertensive controls.…”

Section: Discussionmentioning

confidence: 99%

Serum NT‑proBNP and TUG1 as novel biomarkers for elderly hypertensive patients with heart failure with preserved ejection fraction

Zhang

Jin

2021

Exp Ther Med

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Patients with heart failure with preserved ejection fraction (HFPEF) account for ~50% of all cases of heart failure and their clinical prognosis is poor. The present study attempted to investigate the diagnostic value of circulating long non-coding RNA taurine upregulated gene 1 (TUG1) for HFPEF in subjects with hypertension. Between January 2017 and January 2019, 80 aged/elderly hypertensive patients with or without HFPEF were recruited for the present study. The concentration of N-terminal pro-brain natriuretic peptide (NT-proBNP) in the serum was measured using ELISA and TUG1 expression levels were determined using reverse transcription-quantitative PCR. Echocardiography was used for the determination of cardiac function. The results indicated that the levels of NT-proBNP and TUG1 were increased in the serum of hypertensive patients with HFPEF. Pearson analysis demonstrated that NT-proBNP and TUG1 were positively correlated with the left atrial diameter and negatively correlated with the ratio of the peak flow velocity in the early diastolic phase to the peak flow velocity in the late diastolic phase. In addition, a positive correlation was confirmed between TUG1 and NT-proBNP levels. Receiver operating characteristic curve analysis demonstrated that TUG1 and NT-proBNP were useful biomarkers for the diagnosis of HFPEF. In conclusion, it was observed that NT-proBNP and TUG1 were increased in the serum of hypertensive patients with HFPEF. Furthermore, TUG1 and NT-proBNP were indicated to be useful plasma biomarkers for the diagnosis of HFPEF.

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LncRNA TUG1 contributes to cardiac hypertrophy via regulating miR-29b-3p

Cited by 26 publications

References 38 publications

Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis

Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis

RETRACTED: Long noncoding RNA TUG1 facilitates cell ovarian cancer progression through targeting MiR‐29b‐3p/MDM2 axis

Serum NT‑proBNP and TUG1 as novel biomarkers for elderly hypertensive patients with heart failure with preserved ejection fraction

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